bloodjourГематология и трансфузиологияRussian journal of hematology and transfusiology0234-57302411-3042ООО Издательский дом «Практика»10.35754/0234-5730-2022-67-3-406-418bloodjour-388Research ArticleОБЗОРЫREVIEWSЭндотелиально-тромбоцитарное взаимодействие при сепсисеEndothelial-platelet interaction in sepsishttps://orcid.org/0000-0002-7940-7510ДиваковаЮ. В.DivakovaYu. V.

Дивакова Юлианна Владиславовна, заведующая отделением реанимации и интенсивной терапии

196247, Санкт-Петербург

Yulianna V. Divakova, Head of Department of Reanimation and Intensive Care

196247, St. Petersburg

yulinna-divakova@yandex.ruhttps://orcid.org/0000-0002-5249-4255КолосковА. В.KoloskovA. V.

Колосков Андрей Викторович, доктор медицинских наук, профессор, заведующий кафедрой гематологии и трансфузиологии

191015, Санкт-Петербург

Andrei V. Koloskov, Dr. Sci. (Med.), Professor, Head of the Department of Hematology and Transfusiology

191015, St. Petersburg

Andrei.Koloskov@szgmu.ruСПб ГБУЗ «Городская больница № 26»РоссияSaint Petersburg City Hospital No 26Russian FederationФГБОУ ВО «Северо-Западный Государственный медицинский университет им. И.И. Мечникова» Министерства здравоохранения Российской ФедерацииРоссияNorth-Western State Medical University named after I.I. MechnikovRussian Federation202222102022673406–418Copyright © Дивакова Ю.В., Колосков А.В., 20222022Дивакова Ю.В., Колосков А.В.Divakova Y.V., Koloskov A.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.htjournal.ru/jour/article/view/388Введение

Введение. Эндотелиальные клетки и тромбоциты вовлечены в патогенетические процессы при сепсисе — нерегулируемой реакции организма хозяина в ответ на инфекцию, приводящие, с одной стороны, к развитию протромботической, а с другой стороны — геморрагической готовности.

Цель — обобщить информацию о механизмах межклеточного взаимодействия между эндотелиоцитами и тромбоцитами при сепсисе.

Основные данные

Основные данные. Развитие полиорганной недостаточности, увеличивающей вероятность неблагоприятного исхода сепсиса, отчасти обусловлено дисфункцией эндотелия, а также вовлечением в патогенетический процесс тромбоцитов. В физиологических условиях анатомически и функционально неповрежденный эндотелий важен для предотвращения микрососудистого тромбоза. Хотя тромбоциты в наибольшей степени связаны с гемостазом, они выполняют множество других функций, включая участие в воспалительных процессах через активацию комплемента, взаимодействие с лейкоцитами и моноцитами, участие в защите хозяина от инфекции и регуляции сосудистого тонуса. Процессы, регулирующие гемостаз, развивались как компонент воспалительной реакции на инфекцию. Многие из этих точек взаимодействия возникают на поверхности эндотелиальных клеток, связывая эндотелиоциты и тромбоциты в инициации и регуляции процессов свертывания крови и воспаления. Различные механизмы могут способствовать прямой и непрямой активации тромбоцитов при сепсисе, включая активацию тромбоцитов патогеном, активацию эндотелия и лейкоцитов, вызванную патогеном и воспалением, и активацию тромбоцитов, опосредованную активацией комплемента.

Introduction

Introduction. Endothelial cells and platelets are actively involved in pathogenetic processes in sepsis — an unregulated reaction of the host organism in response to infection, leading, on the one hand, to the development of prothrombotic, and on the other hand, to hemorrhagic readiness.

Aim — to summarize the current information on the mechanisms of intercellular interaction between endotheliocytes and platelets in sepsis.

Main findings

Main findings. The development of multiple organ failure, which increases the likelihood of an unfavorable outcome of sepsis, is partly due to endothelial dysfunction, as well as the involvement of platelets in the pathogenetic process. Under physiological conditions, an anatomically and functionally intact endothelium is important to prevent microvascular thrombosis. Although platelets are most associated with hemostasis, they perform many other functions, including participation in inflammatory processes through complement activation, interaction with leukocytes and monocytes, participation in host defense against infection, and regulation of vascular tone. There is also abundant evidence that suggests that the processes regulating hemostasis evolved as a component of the inflammatory response to infection. Many of these interaction points occur on the surface of endothelial cells, linking these two cell types, endotheliocytes and platelets, in initiating and regulating blood clotting and inflammation. Various mechanisms may contribute to direct and indirect platelet activation in sepsis, including pathogen-induced platelet activation, pathogen- and inflammation-induced endothelial and leukocyte activation, and complement-mediated platelet activation.

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The authors declare that there are no conflicts of interest present.